Evidence map›Paper›PMID 34768890›Full record

ArticleInternational journal of molecular sciences2021

CC16 Regulates Inflammation, ROS Generation and Apoptosis in Bronchial Epithelial Cells during

Sultan Almuntashiri, Yohan Han, Yin Zhu, Saugata Dutta, Sara Niazi, Xiaoyun Wang, Budder Siddiqui, Duo Zhang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.9field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Decoding Host-Pathogen Dynamics inAntibiotics (Basel, Switzerland) · 2026
    Review
  2. Review
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  10. Extracellular vesicle-encapsulated CC16 as novel nanotherapeutics for treatment of acute lung injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2023
    Article
  11. Article
  12. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Sultan AlmuntashiriClinical and Experimental Therapeutics, College of Pharmacy, University of Georgia and Charlie Norwood VA Medical Center, Augusta, GA 30912, USA.ORCID 0000-0003-4353-6043
Yohan HanClinical and Experimental Therapeutics, College of Pharmacy, University of Georgia and Charlie Norwood VA Medical Center, Augusta, GA 30912, USA.
Yin ZhuClinical and Experimental Therapeutics, College of Pharmacy, University of Georgia and Charlie Norwood VA Medical Center, Augusta, GA 30912, USA.
Saugata DuttaClinical and Experimental Therapeutics, College of Pharmacy, University of Georgia and Charlie Norwood VA Medical Center, Augusta, GA 30912, USA.ORCID 0000-0003-4377-5706
Sara NiaziCollege of Pharmacy, University of Georgia, Augusta, GA 30912, USA.
Xiaoyun WangClinical and Experimental Therapeutics, College of Pharmacy, University of Georgia and Charlie Norwood VA Medical Center, Augusta, GA 30912, USA.ORCID 0000-0002-9900-740X
Budder SiddiquiDivision of Infectious Diseases, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.
Duo ZhangClinical and Experimental Therapeutics, College of Pharmacy, University of Georgia and Charlie Norwood VA Medical Center, Augusta, GA 30912, USA.ORCID 0000-0003-0361-4174
University of Georgia · USAugusta University · US

Funding

Lincenc1 regulates the lipopolysaccharide-induced inflammatory response in macrophagesR00HL141685 · NHLBI · UNIVERSITY OF GEORGIA · PI ZHANG, DUO · 2020 to 2022
$743k
Lincenc1 regulates the lipopolysaccharide-induced inflammatory response in macrophagesK99HL141685 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI ZHANG, DUO · 2018 to 2019
$221k
Thyroid Hormone Regulates Immune Response of Macrophages in SepsisR03AI152003 · NIAID · UNIVERSITY OF GEORGIA · PI ZHANG, DUO · 2020 to 2021
$151k
NHLBI NIH HHS K99 HL141685NHLBI NIH HHS R00 HL141685NIAID NIH HHS R03 AI152003NIH HHS NIH/NHLBI R00 HL141685NIH HHS NIH/NIAID R03 AI152003
6 · The paper itself

Abstract

Gram-negative (G-) bacteria are the leading cause of hospital-acquired pneumonia in the United States. The devastating damage caused by G- bacteria results from the imbalance of bactericidal effects and overwhelming inflammation. Despite decades of research, the underlying mechanisms by which runaway inflammation is developed remain incompletely understood. Clara Cell Protein 16 (CC16), also known as uteroglobin, is the major protein secreted by Clara cells and the most abundant protein in bronchoalveolar lavage fluid (BALF). However, the regulation and functions of CC16 during G- bacterial infection are unknown. In this study, we aimed to assess the regulation of CC16 in response to

Indexed as

UteroglobinApoptosisBronchiBronchoalveolar Lavage FluidCytokinesEpithelial CellsImmunity, InnateInflammationKlebsiella pneumoniaeLungNF-kappa BPneumonia, BacterialCytokinesNF-kappa BSCGB1A1 protein, humanUteroglobinbacterial pneumoniacell deathinnate immunitylung injuryNF-κB pathwaySCGB1A1

Identifiers

PMID34768890
PMCPMC8583934
OpenAlexW3208764908

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.